Matrine exerts antitumor activity in cervical cancer by protective autophagy via the Akt/mTOR pathway <i>in vitro</i> and <i>in vivo</i>

Zhang, Fan; Zhang, Hua; Wu, Qian; Xi, Yuyan; Chang, Li‐Te; Wu, Xiaoling

doi:10.3892/ol.2022.13230

Cited by 11 publications

(7 citation statements)

References 61 publications

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“…It is found that matrine inhibits the growth and induces apoptosis of pancreatic cancer cells (Xu et al, 2022). Matrine can promote the autophagy of cervical cancer cells through the Akt/mTOR signaling pathway and can be used as an autophagy inducer of cervical cancer (Zhang et al, 2022). Besides, matrine inhibits the proliferation and migration of colorectal cancer cells and promotes the apoptotic ability of cancer cells (Ren et al, 2022).…”

Section: Discussionmentioning

confidence: 99%

Matrine exerts an anti‐tumor effect via regulating HN1 in triple breast cancer both in vitro and in vivo

Guo,

Yu,

Tang

et al. 2023

Chem Biol Drug Des

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The treatment of triple‐negative breast cancer (TNBC) cannot meet medical needs, and it is urgent to find new drugs for intervention. This study aimed to investigate the anti‐tumor effect of matrine on the proliferation and apoptosis of TNBC cells based on HN1 regulation in vitro and in vivo. TNBC cell lines (MDA‐MB‐453 and HCC‐1806) were treated with varying concentrations of matrine (0, 1.0, 2.0, 3.0, 4.0, and 5.0 mM). CCK‐8, colony formation assay, transwell assay, and flow cytometry assay were employed to detect proliferation, clone formation, invasion, and apoptosis of TNBC cells. Western blot analysis was applied to detect the protein expression of apoptosis HN1. The effects of matrine on tumor growth, protein expression of HN1, and apoptosis in vivo were validated by xenograft tumor models and histology. It was found that matrine inhibited proliferation, colony formation, and invasion and promoted apoptosis of TNBC cells in vitro. HN1 expression was suppressed by matrine. HN1 overexpression perceptibly reversed the above‐mentioned additive effect in vitro. In vivo experiments found that matrine inhibited tumor growth and the expression of HN1 protein but promoted the protein expression of Cleared‐Caspase‐3. Above all, this study demonstrated that matrine inhibited proliferation and promoted apoptosis of TNBC cells via suppressing HN1 expression. Targeting HN1 by matrine may provide new insights into the therapeutic management of patients with TNBC.

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Section: Discussionmentioning

confidence: 99%

Matrine exerts an anti‐tumor effect via regulating HN1 in triple breast cancer both in vitro and in vivo

Guo,

Yu,

Tang

et al. 2023

Chem Biol Drug Des

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“…25 Matrine impaired the proliferation and evoked autophagy in cervical cancer cells by blocking the Akt/mTOR pathway. 26 Ren's team showed that Matrine could weaken the invasiveness and metastasis of breast cancer via suppressing EMT progression through ITGB1. 10 In our study, we also confirmed the anticancer effects of Matrine in HCC.…”

Section: Discussionmentioning

confidence: 99%

“…For instance, Matrine‐inhibited M2‐like macrophage polarization to block the metastasis of lung cancer cells 25 . Matrine impaired the proliferation and evoked autophagy in cervical cancer cells by blocking the Akt/mTOR pathway 26 . Ren's team showed that Matrine could weaken the invasiveness and metastasis of breast cancer via suppressing EMT progression through ITGB1 10 .…”

Section: Discussionmentioning

confidence: 99%

Matrine suppresses hepatocellular carcinoma tumorigenesis by modulating circ_0055976/miR‐1179/lactate dehydrogenase A axis

Chang,

Li,

Huang

et al. 2023

Environmental Toxicology

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BackgroundMatrine has been identified to have anticancer activity in hepatocellular carcinoma (HCC). Circ_0055976 was highly expressed in HCC. Here, we investigated the function and relationship of Matrine and circ_0055976 in HCC tumorigenesis.MethodsCell proliferation and invasion were detected using Cell Counting Kit‐8, 5‐Ethynyl‐2′‐deoxyuridine (EdU), colony formation and transwell assays, respectively. Cell aerobic glycolysis was evaluated by detecting glucose consumption, lactate production, and the ratios of ATP/ADP. Levels of genes and proteins were detected by quantitative real‐time polymerase chain reaction and Western blotting. The target relationship between miR‐1179 and circ_0055976 or lactate dehydrogenase A (LDHA) was analyzed by dual‐luciferase reporter assay. The mouse xenograft model was established to conduct the in vivo assay.ResultsMatrine suppressed HCC cell proliferation, invasion and anaerobic glycolysis in vitro. Circ_0055976 was highly expressed in HCC tissues and cells, and was reduced by Matrine treatment. Moreover, overexpression of circ_0055976 reversed the anticancer effects of Matrine in HCC cells. Mechanistically, circ_0055976/miR‐1179/LDHA formed an axis. Circ_0055976 knockdown or miR‐1179 overexpression impaired HCC cell proliferation, invasion, and anaerobic glycolysis, which were reversed by miR‐1179 inhibition or LDHA overexpression. Meanwhile, forced expression of LDHA abolished the regulatory effects of Matrine on HCC cells. In the clinic, Matrine impeded HCC tumor growth in vivo, and this effect was boosted after circ_0055976 silencing.ConclusionMatrine suppressed HCC cell proliferation, invasion, and anaerobic glycolysis via circ_0055976/miR‐1179/LDHA axis, providing a new insight into the clinical application of Matrine in HCC treatment.

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“…The AKT/mTOR is an intracellular pathway that plays an important role in regulating cell proliferation and migration ( Markowitsch et al, 2022 ; Shao et al, 2022 ; Zhang et al, 2022 ). Thus, the Western blot was used to explore the potential molecular effects of LDOC1 on liver cancer in this study.…”

Section: Discussionmentioning

confidence: 99%

Leucine zipper downregulated in cancer 1 may serve as a favorable prognostic biomarker by influencing proliferation, colony formation, cell cycle, apoptosis, and migration ability in hepatocellular carcinoma

Chen

et al. 2022

Front. Genet.

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Aims: Leucine zipper downregulated in cancer 1 (LDOC1) inhibits tumor growth in several cancers. However, the expression and function of LDOC1 in hepatocellular carcinoma (HCC) remain unknown. In this study, we aimed to investigate how LDOC1 influenced tumor progression and the biological functions of HCC.Methods: The transcription levels of LDOC1 were determined using the GEPIA and UALCAN online databases and a real-time polymerase chain reaction. Western blot and immunohistochemistry were used to validate the protein levels of LDOC1. The online Kaplan-Meier Plotter was applied for survival analysis. Then lentivirus transfection was used to construct LDOC1 exogenous overexpression cell lines. Proliferation, clone formation, cell cycle, apoptosis, and migration assays were performed with the LDOC1-upregulated Huh7 and Hep3B cell lines. The phosphorylated and total levels of AKT and mTOR were determined using a Western blot to explore the potential molecular mechanism of LDOC1.Results: In the GEPIA and UALCAN analyses, LDOC1 was lowly expressed in tumors, had high expression in normal tissue samples (p < 0.05), and negatively correlated with tumor grade progression. The down-regulation of LDOC1 in HCC was validated with real-time polymerase chain reaction, Western blot, and immunohistochemistry (all p < 0.05). LDOC1 transcription levels were negatively associated with overall, progression-free, recurrence-free, and disease-specific survival (all p < 0.05). The functional experiments suggested that the overexpression of LDOC1 contributed to increased G1 and G2 stages in Huh7, while increased G2 stage in Hep3B, and decreased cell proliferation, clone formation, and migration, as well as increased the apoptosis rate compared with the control group (all p < 0.05). Furthermore, LDOC1 up-regulation reduced the p-AKT/AKT and p-mTOR/mTOR, which indicates an inactivation of the AKT/mTOR pathway.Conclusion: The tumor-suppressor LDOC1 varied in HCC and non-HCC tissues, which can serve as a candidate prognostic biomarker. LDOC1 influenced survival by affecting proliferation, colony formation, cell cycle, apoptosis, and migration ability, which might be attributed to the AKT/mTOR inhibition in HCC.

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Matrine exerts antitumor activity in cervical cancer by protective autophagy via the Akt/mTOR pathway in vitro and in vivo

Cited by 11 publications

References 61 publications

Matrine exerts an anti‐tumor effect via regulating HN1 in triple breast cancer both in vitro and in vivo

Matrine exerts an anti‐tumor effect via regulating HN1 in triple breast cancer both in vitro and in vivo

Matrine suppresses hepatocellular carcinoma tumorigenesis by modulating circ_0055976/miR‐1179/lactate dehydrogenase A axis

Leucine zipper downregulated in cancer 1 may serve as a favorable prognostic biomarker by influencing proliferation, colony formation, cell cycle, apoptosis, and migration ability in hepatocellular carcinoma

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